[60] However, these mice also lack CD8 T cells which were shown t

[60] However, these mice also lack CD8 T cells which were shown to be pathogenic in obesity,[50] and their loss alone improves obesity, and so clear conclusions could not

be drawn. To address this issue, Mantell et al. used CD1d−/− mice with normal CD8 levels to measure the contribution of iNKT cells to obesity.[61] Like other studies, Mantell et al. found that iNKT cells were decreased in the liver of obese mice but found an increase in adipose iNKT cells in obesity, unlike the majority of other studies. One caveat is that this study used NK1.1+ CD3+ as surrogate markers for iNKT cells, which also detects other T cells that are not iNKT cells, particularly in adipose tissue where NK1.1 is not expressed on a substantial proportion of iNKT cells. It may also detect non-invariant type II NKT cells, or MHC-restricted T cells, which Selleckchem Ensartinib have been shown to up-regulate NK markers when activated,[62] and these could be possible Selleckchem CHIR 99021 explanations for an increase in NK1.1+ T cells in obesity. Nevertheless, in this study, obese CD1d−/− mice were not significantly different from obese wild-type mice in terms of weight gain and metabolic parameters.[61] Boes and colleagues found that iNKT-deficient mice had increased adipocyte size

and insulin resistance, and their depletion increased insulin resistance. They also found that CD1d−/− mice on an HFD had increased insulin resistance, but they did not observe any difference in weight gain between wild-type and NKT-deficient mice on an HFD. However, Kotas et al. found that iNKT-deficient mice

were metabolically normal on a standard diet, but CD1d−/− mice had mildly but significantly impaired glucose tolerance and increased insulin resistance on an HFD.[63] This study particularly focused on hepatic iNKT cells, which they found were reduced in obesity, and mice lacking iNKT cells had increased liver triglycerides and worse hepatic steatosis. However, many of these features were not seen in Ja18−/− mice on HFD, suggesting that either www.selleck.co.jp/products/Metformin-hydrochloride(Glucophage).html other CD1d-restricted T cells are responsible for the worsened metabolism and steatosis, or that Ja18−/− mice displayed some compensation for the iNKT cell deficiency. Hams et al. also found that while iNKT cells positively regulated obesity and metabolism and were depleted in obese mice, they did not find any differences in weight or glucose homeostasis in CD1d−/− or Ja18−/− mice.[64] This series of studies suggests that deficiency in iNKT cells from birth does not alter weight gain and metabolism, yet iNKT deficiency from birth resulted in excess weight and impaired metabolism on a normal diet. On the other hand, our laboratory, Qi and colleagues, and Kim and colleagues all found that mice deficient in iNKT cells had accelerated obesity and had significantly more severe glucose impairment and insulin resistance on an HFD.

Related posts:

  1. At the functional level, rat splenocytes and IHLs have been shown
  2. Without a doubt, serum IgG anti phospholipid antibody ranges have
  3. Dyphylline pancreatic cells of mice results in enhanced insulin secretion
  4. The typical TSHR protein degree in obese mice was drastically ele
  5. Obesity-induced weight gain, increase in fasting blood glucose an
This entry was posted in Antibody. Bookmark the permalink.

Leave a Reply

Your email address will not be published. Required fields are marked *

*

You may use these HTML tags and attributes: <a href="" title=""> <abbr title=""> <acronym title=""> <b> <blockquote cite=""> <cite> <code> <del datetime=""> <em> <i> <q cite=""> <strike> <strong>